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目的探讨固有免疫信号通路分子IRAK-M在TLR9信号诱导肝组织淋巴细胞浸润过程中的作用。方法应用野生型B6小鼠及IRAK-M基因敲除小鼠,腹腔注射TLR9配体CpG寡核苷酸激活肝内TLR9信号系统,提取小鼠肝内浸润淋巴细胞,并采用流式细胞术检测肝内浸润不同淋巴细胞群的比率及细胞因子的表达情况。结果 CpG ODN激活TLR9信号通路后,IRAK-M基因敲除小鼠肝内浸润CD4+和CD8+T细胞比率较野生型B6小鼠显著增加[CD4+:(22.50±0.73)% vs. (20.03±0.75)%;CD8+:(17.83±0.67)%vs.(15.55±0.75)%;P均<0.05];肝内淋巴细胞细胞因子白细胞介素-6(IL-6)和肿瘤坏死因子(TNF-α)合成增加[IL-6:(1.91±0.26)% vs. (0.93±0.12)%;TNF-α:(13.23±1.23)% vs. (8.16±0.66)%;P均<0.01]。结论 IRAK-M具有负调节肝内TLR9信号系统的作用。
Objective To investigate the role of IRAK-M, an innate immune signaling pathway, in the induction of lymphocyte infiltration in liver tissue by TLR9 signaling. Methods Wild type B6 mice and IRAK-M knockout mice were used. TLR9 ligand CpG oligonucleotide was injected intraperitoneally to activate TLR9 signaling system in liver, and the intrahepatic infiltrating lymphocytes were extracted and detected by flow cytometry Intrahepatic infiltration of different lymphocyte populations and the expression of cytokines. Results The ratio of infiltrating CD4 + and CD8 + T cells in IRAK-M knockout mice was significantly increased compared with wild-type B6 mice after stimulation of TLR9 signaling pathway by CpG ODN [CD4 +: (22.50 ± 0.73)% vs. (20.03 ± 0.75 ); CD8 +: (17.83 ± 0.67)% vs (15.55 ± 0.75)%; all P <0.05]. The intrahepatic lymphocyte cytokines interleukin-6 (IL-6) and tumor necrosis factor ) (IL-6: (1.91 ± 0.26)% vs. (0.93 ± 0.12)%; TNF-α: (13.23 ± 1.23)% vs. (8.16 ± 0.66)%, P <0.01]. Conclusion IRAK-M can negatively regulate the TLR9 signal system in the liver.